Investigation of the role of ocular surface conditions in blinking.

This thesis considers the question: What roles do the tear film and corneal nerves play in the normal blink mechanism. The hypothesis proposed is that tear film thinning, which occurs prior to full break-up, allows increased evaporation of the tear film. The evaporation produces a localised reduction in the tear film temperature, which is then detected by the temperature sensitive nerves in the corneal epithelium. To test this hypothesis, a series of experiments was completed. The first study, which investigated the pattern of diurnal change in corneal sensitivity, revealed that corneal sensitivity increases during the day following post-sleep eyelid opening to reach a plateau approximately five hours after eye opening (Kruskall-Wallis, 0.05). The second study assessed corneal nerve function under anaesthesia produced by 0.5% Proxymetacaine Hydrochloride. Onset of anaesthesia was observed within 2 minutes (Wilcoxon matched pairs test, >0.05), with a maximum of anaesthesia reached at 15 minutes post-instillation (Wilcoxon matched pairs test, >0.05). Corneal sensitivity did not return to pre-instillation levels at 60 minutes post-instillation (Wilcoxon matched pairs test, 0.05). The third study assessed the effect of iris colour and ethnic origin on corneal sensitivity, skin sensitivity, tear film stability and blink rate. The study showed that corneal sensitivity for a cooling stimulus was affected by iris colour and ethnic origin (Kruskall-Wallis, >0.05): as iris pigmentation increases, corneal sensitivity decreases. Although statistically tear film stability was found to be influenced by iris colour, no clear pattern of change was associated with iris colour (Kruskall-Wallis, p>0.05). Tear film stability was not affected by ethnic origin (Kruskall-Wallis, p>0.05). Blink rate was significantly correlated to tear film stability (Spearman, r = -0.536, >0.05). The fourth study considered the relationship between blink rate, corneal sensitivity, tear film stability, anaesthesia, ocular surface temperature and ocular surface evaporation. Tear film stability was strongly correlated to blink rate, with the blink rate increasing as tear film stability decreases (Spearman, r = 0.926, >0.05). Corneal sensitivity was significantly correlated to corneal sensitivity, but only at low corneal sensitivity levels. Blocking corneal sensitivity by anaesthesia, the blink rate was significantly reduced, suggesting that corneal sensitivity is involved in the mechanism controlling normal involuntary blinking (Wilcoxon matched pairs test, >0.05). Tear film evaporation from the ocular surface was not correlated to the blink frequency (Spearman, r = -0.381, p>0.05). The amount of temperature cooling at the inter-blink interval was not correlated to blink rate (Spearman, r = 0.241, p>0.05). The final experimental study examined involuntary blinking with contact lens wear discomfort. There was a significant increase in the blink rate with increasing discomfort (Kruskall-Wallis, p<0.05). Subjects experiencing discomfort had a less stable tear-film, both with (Mann Whitney test, p>0.05) and without (Mann Whitney test, >0.05) contact lens wear, and had an elevated blink-rate compared to subjects experiencing comfort (Mann Whitney test, >0.05). Ocular surface discomfort was not related to an elevated corneal sensitivity (Mann-Whitney test, p>0.05). These series of studies showed that tear film stability and corneal sensitivity are involved in the blink mechanism, providing strong evidence that normal involuntary blinking is affected by sensory stimuli arising from the exposed ocular surface